Findings of Research Misconduct, 48709-48713 [2020-17602]

Download as PDF 48709 Federal Register / Vol. 85, No. 156 / Wednesday, August 12, 2020 / Notices health care facilities searching for potential candidates to fill open health care job opportunities at their sites. Burden Statement: Burden in this context means the time expended by persons to generate, maintain, retain, disclose or provide the information requested. This includes the time needed to review instructions; to develop, acquire, install and utilize technology and systems for the purpose of collecting, validating and verifying information, processing and maintaining information, and disclosing and providing information; to train personnel and to be able to respond to a collection of information; to search data sources; to complete and review the collection of information; and to transmit or otherwise disclose the information. The total annual burden hours estimated for this ICR are summarized in the table below. TOTAL ESTIMATED ANNUALIZED BURDEN HOURS Number of respondents Form name Total responses Average burden per response (in hours) Total burden hours Account Creation ................................................................. Complete Profile .................................................................. 15,600 9,400 1 1 15,600 9,400 .08 1 1,248 9,400 Total .............................................................................. 1 15,600 ........................ 15,600 ........................ 10,648 1 The 9,400 respondents who complete their profiles are a subset of the 15,600 respondents who create accounts. HRSA specifically requests comments on (1) the necessity and utility of the proposed information collection for the proper performance of the agency’s functions, (2) the accuracy of the estimated burden, (3) ways to enhance the quality, utility, and clarity of the information to be collected, and (4) the use of automated collection techniques or other forms of information technology to minimize the information collection burden. Maria G. Button, Director, Executive Secretariat. [FR Doc. 2020–17635 Filed 8–11–20; 8:45 am] BILLING CODE 4165–15–P DEPARTMENT OF HEALTH AND HUMAN SERVICES Office of the Secretary Findings of Research Misconduct Office of the Secretary, Health and Human Services (HHS). ACTION: Notice. AGENCY: Findings of research misconduct have been made against Zhiwei Wang, M.D. (Respondent), former postdoctoral fellow, Department of Pathology, Karmanos Cancer Institute, Wayne State University (WSU). Dr. Wang engaged in research misconduct in research supported by U.S. Public Health Service (PHS) funds, specifically National Cancer Institute (NCI), National Institutes of Health (NIH), grants P20 CA101936, P30 CA022453, R01 CA075059, R01 CA083695, R01 CA101870, R01 CA109389, R01CA131151, R01 CA132794, and U19 CA113317. The administrative actions, including debarment for a period of ten (10) years, SUMMARY: khammond on DSKJM1Z7X2PROD with NOTICES Number of responses per respondent VerDate Sep<11>2014 16:37 Aug 11, 2020 Jkt 250001 were implemented beginning on July 21, 2020, and are detailed below. FOR FURTHER INFORMATION CONTACT: Elisabeth A. Handley, Director, Office of Research Integrity, 1101 Wootton Parkway, Suite 240, Rockville, MD 20852, (240) 453–8200. SUPPLEMENTARY INFORMATION: Notice is hereby given that the Office of Research Integrity (ORI) has taken final action in the following case: Zhiwei Wang, M.D., Wayne State University: Based on the report of an investigation conducted by WSU and additional analysis conducted by ORI in its oversight review, ORI found that Dr. Zhiwei Wang, former postdoctoral fellow, Department of Pathology, Karmanos Cancer Institute, WSU, engaged in research misconduct in research supported by PHS funds, specifically NCI, NIH, grants P20 CA101936, P30 CA022453, R01 CA075059, R01 CA083695, R01 CA101870, R01 CA109389, R01CA131151, R01 CA132794, and U19 CA113317. ORI found that Respondent engaged in research misconduct by knowingly, intentionally, and/or recklessly falsifying data that were included in grant applications R01 CA120008, R01 CA131151, and R01 CA131456 submitted to NCI, NIH; his 2006 Ph.D. dissertation (hereafter referred to as the ‘‘Dissertation’’); and the following published papers: • Activated K-Ras and INK4a/Arf deficiency promote aggressiveness of pancreatic cancer by induction of EMT consistent with cancer stem cell phenotype. J Cell Physiol. 2013 Mar;228(3):556–62 (hereafter referred to as ‘‘J Cell Physiol. 2013’’). Erratum in: J Cell Physiol. 2014 Aug;229(8):1118. Retraction in: J Cell Physiol. 2016 Oct;231(10):2304. PO 00000 Frm 00045 Fmt 4703 Sfmt 4703 • Activated K-ras and INK4a/Arf deficiency cooperate during the development of pancreatic cancer by activation of Notch and NF-kB signaling pathways. PLoS One 2011;6(6):e20537 (hereafter referred to as ‘‘PLoS One 2011’’). Erratum in: PLoS One 2014;9(6):e101032. Retraction in: PLoS One. 2018 Oct 2;13(10):e0205289. • Down-regulation of Notch-1 is associated with Akt and FoxM1 in inducing cell growth inhibition and apoptosis in prostate cancer cells. J Cell Biochem. 2011 Jan;112(1):78–88 (hereafter referred to as ‘‘J Cell Biochem. 2011’’). Retraction in: J Cell Biochem. 2016 Aug;117(8):1962. • Down-regulation of Notch-1 and Jagged-1 inhibits prostate cancer cell growth, migration and invasion, and induces apoptosis via inactivation of Akt, mTOR, and NF-kB signaling pathways. J Cell Biochem. 2010 Mar 1;109(4):726–36 (hereafter referred to as ‘‘J Cell Biochem. 2010’’). Retraction in: J Cell Biochem. 2016 Aug;117(8):1960. • TW–37, a small-molecule inhibitor of Bcl-2, inhibits cell growth and invasion in pancreatic cancer. Int J Cancer 2008 Aug 15;123(4):958–66 (hereafter referred to as ‘‘Int J Cancer 2008’’). Retraction in: Int J Cancer. 2016 Nov 1;139(9):2146. • Induction of growth arrest and apoptosis in human breast cancer cells by 3,3-diindolylmethane is associated with induction and nuclear localization of p27kip. Mol Cancer Ther. 2008 Feb;7(2):341–9 (hereafter referred to as ‘‘Mol Cancer Ther. 2008’’). • Down-regulation of platelet-derived growth factor-D inhibits cell growth and angiogenesis through inactivation of Notch-1 and nuclear factor-kB signaling. Cancer Res. 2007 Dec 1; 67(23):11377– 85 (hereafter referred to as ‘‘Cancer Res. E:\FR\FM\12AUN1.SGM 12AUN1 khammond on DSKJM1Z7X2PROD with NOTICES 48710 Federal Register / Vol. 85, No. 156 / Wednesday, August 12, 2020 / Notices 2007c’’). Retraction in: Cancer Res. 2018 Sep 15;78(18):5469. • Down-regulation of Forkhead Box M1 transcription factor leads to the inhibition of invasion and angiogenesis of pancreatic cancer cells. Cancer Res. 2007 Sep 1;67(17):8293–300 (hereafter referred to as ‘‘Cancer Res. 2007b’’). Retraction in: Cancer Res. 2018 Sep 15; 78(18):5470. • Inhibition of angiogenesis and invasion by 3,3′-diindolylmethane is mediated by the nuclear factor-kB downstream target genes MMP–9 and uPA that regulated bioavailability of vascular endothelial growth factor in prostate cancer. Cancer Res. 2007 Apr 1;67(7):3310–9 (hereafter referred to as ‘‘Cancer Res. 2007a’’). Retraction in: Cancer Res. 2018 Sep 15; 78(18):5471. • Notch-1 down-regulation by curcumin is associated with the inhibition of cell growth and the induction of apoptosis in pancreatic cancer cells. Cancer 2006 Jun 1;106(11):2503–13 (hereafter referred to as ‘‘Cancer 2006’’). Retraction in: Cancer 2016 Oct 15;122(20):3247. • Epidermal growth factor receptorrelated protein inhibits cell growth and invasion in pancreatic cancer. Cancer Res. 2006 Aug 1;66(15):7653–60 (hereafter referred to as ‘‘Cancer Res. 2006b’’). Retraction in: Cancer Res. 2018 Sep 15;78(18):5474. • Inhibition of nuclear factor kappab activity by genistein is mediated via Notch-1 signaling pathway in pancreatic cancer cells. Int J Cancer 2006 Apr 15;118(8):1930–6 (hereafter referred to as ‘‘Int J Cancer 2006’’). Erratum in: Int J Cancer 2014 Apr 15;134(8):E3. Retraction in: Int J Cancer 2016 Nov 1;139(9):2145. • Down-regulation of Notch-1 inhibits invasion by inactivation of nuclear factor-kappab, vascular endothelial growth factor, and matrix metalloproteinase-9 in pancreatic cancer cells. Cancer Res. 2006 Mar 1;66(5):2778–84 (hereafter referred to as ‘‘Cancer Res. 2006a’’). Retraction in: Cancer Res. 2018 Sep 15;78(18):5476. • Down-regulation of Notch-1 contributes to cell growth inhibition and apoptosis in pancreatic cancer cells. Mol Cancer Ther. 2006 Mar;5(3):483–93 (hereafter referred to as ‘‘Mol Cancer Ther. 2006’’). Retraction in: Mol Cancer Ther. 2018 Oct;17(10):2268. ORI found by a preponderance of evidence that Respondent engaged in research misconduct by intentionally, knowingly, and/or recklessly falsifying and/or fabricating images representing protein expression, invasion and migration assays, and electrophoretic mobility shift assays (EMSA) in experiments designed to identify VerDate Sep<11>2014 16:37 Aug 11, 2020 Jkt 250001 underlying mechanisms controlling cell proliferation, differentiation, and apoptosis in cancer so that novel targeted therapeutic agents could be identified. Specifically, Respondent reused and relabeled: • The same protein bands to represent experimental conditions in: —Figure 6D (upper panel) in the Dissertation; Figure 1D (upper panel) in Mol Cancer Ther. 2006: Downregulation of Notch-1 expression by siRNA in BxPC–3, HPAC, and PANC– 1 cells —Figure 6D (lower panel) in the Dissertation; Figure 1D (lower panel) in Mol Cancer Ther. 2006: Upregulation of Notch-1 expression by cDNA transfection in BxPC–3, HPAC, and PANC–1 cells —Figure 8A in Mol Cancer Ther. 2006: Down-regulation of Notch-1 expression by genistein and Notch-1 siRNA —Figure 4 in Int J Cancer 2006: Downregulation of Notch-1 expression by genistein and Notch-1 siRNA • inhibition of Bcl-XL (0–72 hours with genistein) in BxPC–3 cells in Figure 20 in the Dissertation, Figure 7B in Mol Cancer Ther. 2006, and Figure 3C in Int J Cancer 2006 to also represent: —Inhibition of Bcl-XL (0–13 uM curcumin) in PANC–1 cells in Figure 3D in Cancer 2006 —inhibition of Notch-1 expression (ERRP and Notch-1 siRNA transfection) in BxPC–3 cells in Figure 5A in Cancer Res. 2006b • inhibition of Hes-1 (0–72 hours genistein) in BxPC–3 cells in Figure 7B in Mol Cancer Ther. 2006 to also represent: —Inhibition of Cyclin D1 (0–72 hours with genistein) in BxPC–3 cells in Figure 20 in the Dissertation and Figure 3C in Int J Cancer 2006 —inhibition of Cyclin D1 (0–13 uM curcumin in PANC–1 cells) in Figure 3D in Cancer 2006 • inhibition of Cyclin D1 (0–72 hours with genistein) in BxPC–3 cells in Figure 7B in Mol Cancer Ther. 2006 to also represent inhibition of Hes-1 (0–72 hours with genistein) in BxPC– 3 cells in Figure 20 in the Dissertation and Figure 3C in Int J Cancer 2006 • expression of Bcl-2 in control and Notch-1 siRNA transfected pancreatic cell lines (BxPC–3, HPAC) in Figure 10 in the Dissertation and Figure 5 in Mol Cancer Ther. 2006 to represent expression of Notch-1 in control and PDGF–D siRNA transfected pancreatic cells in Figure 4A in Cancer Res. 2007c. PO 00000 Frm 00046 Fmt 4703 Sfmt 4703 • representing expression of Cyclin D1 and Bcl-XL in control and Notch-1 siRNA transfected pancreatic cell lines (BxPC–3, HPAC, PANC–1) in Figure 10 in the Dissertation and Figure 5D in Mol Cancer Ther. 2006 to represent expression of Hes-1 and Cyclin D1 in control and ERRPincubated pancreatic cells in Figure 2C in Cancer Res. 2006b • expression of p27 in control and Notch-1 siRNA transfected pancreatic cell lines (HPAC) in Figure 10 in the Dissertation and Figure 5 in Mol Cancer Ther. 2006 to represent VEGF protein expression in control and Notch-1 plasmid transfected BxPC–3 cells in Figure 4B in Cancer Res. 2006a • expression of Cyclin D1 in control and Notch-1 siRNA transfected pancreatic cell lines in Figure 10 in the Dissertation and Figure 5 in Mol Cancer Ther. 2006 to represent the expression of uPAR genes in control siRNA and FoxM1 siRNA transfected pancreatic cancer cells in Figure 5B in Cancer Res. 2007b • expression of Hes-1 in control and ERRP-incubated pancreatic cancer cells in Figure 2C in Cancer Res. 2006b to represent the expression of uPAR genes in control siRNA and FoxM1 siRNA transfected pancreatic cancer cells in Figure 5B in Cancer Res. 2007b • expression of Hes-1 in control and ERRP-incubated pancreatic cells in Figure 2C in Cancer Res. 2006b to represent control, TGF-a, and TGFa+ERRP effects on Notch-1 activation in BxPC–3 cells in Figure 2D in Cancer Res. 2006b • inhibition of Bcl-XL, Hes-1, and Cyclin D protein expression by genistein in BxPC–3 cells at 0, 24, 48, and 72 hours in three different experiments in Figure 7B in Mol Cancer Ther. 2006 to represent the same protein expressions in one experiment in Figure 3C in Int J Cancer 2006 • up-regulation of Notch-1 in cDNAtransfected BxPC–3 cells in Figure 5C in Cancer Res. 2006b to also show that ERRP inhibits the expression of MMP–9 in Figure 6 in Cancer Res. 2006b • expression of Notch-1 when transfected with Jagged-1 siRNA in PC–3 cells in Figure 5A in J Cell Biochem. 2010 to also show the expression of Notch-1 when transfected with Notch-1 siRNA in C4–2B cells in Figure 3A in J Cell Biochem. 2011 • expression of Notch-4 in a genetically modified mouse model (KCI) in Figure 1D in PLoS One 2011 to also E:\FR\FM\12AUN1.SGM 12AUN1 khammond on DSKJM1Z7X2PROD with NOTICES Federal Register / Vol. 85, No. 156 / Wednesday, August 12, 2020 / Notices show the expression of Bcl-2 in the same mouse model in Figure 3A in the same paper • expression of EZH2 in IC, KC, and KCI transgenic mice to also represent the expression of E-cadherin in the same mouse types in Figure 4B in J Cell Physiol. 2013 Respondent reused and relabeled one set of b-actin bands to represent loading controls for the following experiments showing: • Inhibition of VEGF in Notch-1 siRNA transfected BxPC–3 cells in Figure 16B in the Dissertation • inhibition of cyclin D1 in genisteintreated BxPC–3 cells over time in Figure 7B in Mol Cancer Ther. 2006 • inhibition of Notch-1 in genisteintreated BxPC–3 cells over time in Figure 8A in Mol Cancer Ther. 2006 • down-regulation of MMP–9 expression in Notch-1 siRNA transfected BxPC–3 cells in Figure 17A (left) in the Dissertation and Figure 3B in Cancer Res. 2006a • up-regulation by cDNA transfection and down regulation by Notch-1 siRNA transfection in BcPC–3 cells in Figure 4B in Cancer Res. 2006a • down-regulation of MMP–9 in ICNtransfected BxPC–3 cells in Figure 15B in the Dissertation and Figure 5A in Cancer Res. 2006a • inhibition of Notch-1, Hes-1, Cyclin D1, and Bcl-XL protein expression after 72 hours of curcumin treatment in pancreatic cancer cells in Figure 3D in Cancer 2006 • down-regulation of Notch-1 expression by curcumin and Notch-1 siRNA in Notch-1 siRNA-transfected BxPC–3 cells in Figure 5A in Cancer 2006 • down-regulation of Notch-1 expression in Notch-1 siRNAtransfected BxPC–3 cells compared with control in Figure 5A in Cancer Res. 2006b • inhibition of Hes-1, Cyclin D1 and Bcl-xL in genistein-treated BxPC–3 cells over time in Figure 20C in the Dissertation and Figure 3C in Int J Cancer 2006 • inhibition of Bcl-xL, Bcl-2, Cyclin D1, COX–2, Survivin and MMP–9 protein expression by Notch-1 siRNA in BxPC–3 cells in Figure 6A in Int J Cancer 2006 • inhibition of IKKa and pIkBa protein expression by Notch-1 siRNA in BxPC–3 cells in Figure 6B in Int J Cancer 2006 Respondent reused and relabeled a second set of b-actin bands to represent loading controls for the following experiments showing: • Increasing inhibition of Notch-1 by 25 mmol/l genistein at 24, 48, and 72 VerDate Sep<11>2014 16:37 Aug 11, 2020 Jkt 250001 hours in BxPC–3 cells in Figure 20A in the Dissertation, Figure 7B in Mol Cancer Ther. 2006, and Figure 3A in Int J Cancer 2006 • up-regulation of Notch-1 in Notch-1 cDNA transfected BxPC–3 cells, with or without 10 mmol/l curcumin, in Figure 6A in Cancer 2006 Respondent reused and relabeled a third set of b-actin bands to represent loading controls for the following experiments showing: • The level of expression of seven known G0-G1 cell cycle regulatory factors in Figure 10 in the Dissertation and Figure 5 in Mol Cancer Ther. 2006 • overexpression of Notch-1 in Notch-1 cDNA transfected BxPC–3 cells in Figure 22A in the Dissertation and Figure 9A in Mol Cancer Ther. 2006 • inhibition of NF-kB target gene expression by Notch-1 siRNA in BxPC–3 cells in Figure 23A in the Dissertation • inhibition of IKKa and pIkBa protein expression by Notch-1 siRNA in BxPC–3 pancreatic cancer cells in Figure 23B the Dissertation • overexpression of Notch-1 in Notch-1 siRNA–transfected BxPC–3 cells in Figure 1C in Cancer Res. 2006a • down-regulation of VEGF by siRNA transfection in ICN-transfected BxPC– 3 cells in Figure 5A (right) in Cancer Res. 2006a • up-regulation of Notch-1 in cDNAtransfected and cDNA and ERRP transfected BxPC–3 cells in Figure 5C in Cancer Res. 2006b • inhibition of MMP-2, MMP-9, and uPAR genes by FoxM1 siRNA in BxPC–3, HPAC, and PANC–1 cells in Figure 5B in Cancer Res. 2007b Respondent reused and relabeled a fourth set of b-actin bands to represent loading controls for the following experiments showing: • FoxM1 expression in AsPC–1, BxPC– 3, Colo-357, HPAC, L3.6pl, MIA PaCa and PANC–1 cells in Figure 1A in Cancer Res. 2007b • PDGF–D expression in PDGF–D cDNA transfected BxPC–3, Colo-357, and MIA PaCa cells in Figure 2C in Cancer Res. 2007c • Bcl-2 expression in AsPC–1, BxPC–3, Colo-357, HPAC, L3.6pl, MIA PaCa and PANC–1 cells in Figure 1C in Int J Cancer 2008 Respondent reused and relabeled a fifth set of b-actin bands to represent loading controls for the following experiments showing: • Down regulation of PDFG–D expression by PDGF–D siRNA in BcPC–3, HPAC, and Colo-357 cells PO 00000 Frm 00047 Fmt 4703 Sfmt 4703 48711 and up-regulation of PDGF–D expression by PDGF–D cDNA in BxPC–3, Colo-357, and MIA PaCa cells in Figure 2C in Cancer Res. 2007c • inhibition of Notch-1 expression by PDGF–D siRNA in BxPC–3, HPAC, and Colo-357 cells in Figure 4A in Cancer Res. 2007c Respondent reused and relabeled a sixth set of b-actin bands to represent loading controls for the following experiments showing: • Up-regulation of Notch-1 expression by cDNA in BxPC–3, HPAC, and PANC–1 cells in Figure 6D (bottom) in the Dissertation and Figure 1D in Mol Cancer Ther. 2006 • down-regulation of Notch-1 expression by Notch-1 siRNA and genistein in BxPC–3 cells in Figure 21 in the Dissertation and Figure 4A in Int J Cancer 2006 Respondent reused and relabeled a seventh set of b-actin bands to represent loading controls for the following experiments showing: • Down-regulation of Notch-1 expression by Notch-1 siRNA in BxPC–3, HPAC, and PANC–1 cells in Figure 6D (top) in the Dissertation and Figure 1D in Mol Cancer Ther. 2006 • expression of Notch-1, Hes-1, and Cyclin D1 after incubation with recombinant ERRP in BxPC–3, HPAC, and PANC–1 cells in Figure 2C in Cancer Res. 2006b • effects of ERRP, Erbitux, or Herceptin followed by exposure to TGF-a or HB–EGF on Notch-1 expression in BxPC–3 cells in Figure 2D in Cancer Res. 2006b • down-regulation of FoxM1 expression by FoxM1 siRNA in BxPC–3, HPAC, and PANC–1 cells in Figure 1D in Cancer Res. 2007b • the level of expression of seven known G0-G1 cell cycle regulatory factors (Survivin, cdc25A, p27, p21, Cyclin D1, Cyclin B, and CDK2) in Figure 4C in Cancer Res. 2007b Respondent reused and relabeled: • Invasion assay results showing a high level of penetration of Notch-1 cDNAtransfected cells through a Matrigel matrix in Figure 1D in Cancer Res. 2006a, to also represent control siRNA-transfected cells (controls) not transfected with MMP–9 or VEGF siRNA in Figure 5B in Cancer Res. 2006a • sections from one image of an invasion assay to show a lower level of penetration of C4–2B cells through a Matrigel matrix after treatment with 10 mmol/L of B–DIM than in the control condition (DMSO) in Figure 6B in Cancer Res. 2007a E:\FR\FM\12AUN1.SGM 12AUN1 khammond on DSKJM1Z7X2PROD with NOTICES 48712 Federal Register / Vol. 85, No. 156 / Wednesday, August 12, 2020 / Notices • sections from one image to show the penetration of both control and ERRPtreated HPAC cells through a Matrigel matrix in Figure 4 in Cancer Res. 2006b • one image to show the penetration of ERRP-treated PANC–1 cells through a Matrigel matrix in Figure 4 in Cancer Res. 2006b to also show the penetration of TW–37 treated Colo357 cells in Figure 5b in Int J Cancer 2008 • images of assays of endothelial tube formation after HUVACs were trypsinized and seeded with control siRNA transfected BxPC–3 or HPAC cells in Figure 6c in Cancer Res. 2007b • a single gel shift band showing the no treatment control condition (CS) in an EMSA assay using BxPC–3 cells showing down regulation of NF-kB DNA binding by Notch-1 siRNA in Figures 11A and 14A in the Dissertation to also show: —The control conditions (CP) in assays showing activation of NF-kB binding activity by Notch-1 plasmid (cDNA) transfection in Figures 11A and 14A in the Dissertation —inhibition of NF-kB DNA binding activity after treatment with 25 mM genistein for 48 hours in Figure 19B in the Dissertation • a single gel shift band showing the effect of Notch-1 siRNA transfection of BxPC–3 cells, showing inhibition of NF-kB DNA binding activity in Figures 11A and 14A in the Dissertation to also show NF-kB binding activity in BxPC–3 cells after treatment with 25 mM genistein in Figure 22C in the Dissertation • a single gel shift band showing the effect of Notch-1 cDNA transfection of BxPC–3 cells, showing activation of NF-kB DNA binding activity in Figures 11A and 14A in the Dissertation to also show NF-kB binding activity in BxPC–3 cells in the no treatment control condition in an experiment showing the effect of genistein on binding in Figure 22C in the Dissertation • a single gel shift band showing the no treatment control condition in an EMSA assay using HPAC cells showing down regulation of NF-kB DNA binding by Notch-1 siRNA in Figure 11A in the Dissertation to also show the no treatment control condition in the activation of NF-kB DNA binding after transfection with Notch-1 cDNA • a single gel shift band showing the effect of 0 mM genistein on NF-kB binding activity in BxPC3 cells in VerDate Sep<11>2014 16:37 Aug 11, 2020 Jkt 250001 Figure 19A the Dissertation to also show the effect of: —25 mM of genistein for 0 hours in HPAC cells in Figure 19B in the Dissertation —Notch-1 cDNA on NF-kB binding activity in Figure 22C in the Dissertation • a single gel shift band showing the effect of 10 mM genistein on NF-kB binding activity in BxPC3 cells in Figure 19A in the Dissertation to also show the effect of: —25 mM genistein for 24 hours in HPAC cells in Figure 19B in the Dissertation —Notch-1 cDNA plus 25 mM genistein on NF-kB binding activity in Figure 22C in the Dissertation • a single gel shift band showing the effect of Bcl-2 siRNA transfection of Colo-357 cells showing downregulation of NF-kB DNA binding activity to also show the same effect with 500 nM TW–37 on Colo-357 cells in Figure 3a in Int J Cancer 2008 Respondent reused and relabeled images representing the retinoblastoma control protein (Rb) levels from one EMSA in multiple figures. Respondent used the same loading controls assay blots, in different orders with some flipped horizontally, showing: • Down-regulation of Notch-1 gene expression by Notch-1 siRNA in siRNA- and cDNA-transfected BxPC– 3, HPAC, and PANC–1 cells in Figure 11 in the Dissertation and Figure 6 in Mol Cancer Ther. 2006 • down-regulation of Notch-1 by genistein in BxPC–3 cells in Figure 7E in Mol Cancer Ther. 2006 • Notch-1 induced NF-kB DNA binding in Figure 14 in the Dissertation and Figure 2 in Cancer Res. 2006a • down-regulation of Notch-1 by curcumin in BxPC–3 and PANC–1 cells in Figures 4, 5D, and 6D in Cancer 2006 • inhibition of NF-kB activation in three types of pancreatic cancer cells (BxPC–3, HPAC, PANC–1) in Figure 3A in Cancer Res. 2006b • inhibition of NF-kB DNA binding activity by genistein (by dose and time) in Figure 19 in the Dissertation and Figure 2 in Int J Cancer 2006 • inhibition of NF-kB DNA-binding activity by Notch-1 siRNA in BxPC– 3 pancreatic cancer cells in Figure 22 in the Dissertation and Figure 5 in Int J Cancer 2006 • decreased NF-kB DNA-binding activity through down-regulation of PDGF–D by siRNA transfection in BxPC–3, HPAC, and Colo-357 pancreatic cancer cells, activation of NF-kB DNA binding activity in PO 00000 Frm 00048 Fmt 4703 Sfmt 4703 BxPC3, Colo-357, and MIA PaCa pancreatic cancer cells in Figure 5A in Cancer Research 2007c • differences in NF-kB activation in a panel of pancreatic cancer cell lines (AsPC–1, BxPC–3, Colo-357, HPAC, L3.6pl, MIA PaCa, PANC–1 in Figure 1d in Int J Cancer 2008 • inhibition of NF-kB activation by Bcl2 siRNA in Colo-357 cells and by TW–37 (by dose and time) in Colo357 and BXPC–3 pancreatic cancer cells in Figure 3a in Int J Cancer 2008 • inhibition of NF-kB activation by TW–37 in Colo-357 tumor xenografts from SCID mice in Figure 6c in Int J Cancer 2008 In addition, Respondent used these same images to represent b-actin in a figure showing that FoxM1 protein levels were up-regulated by FoxM1 cDNA plasmid in AsPC–1, PANC–1, and Colo-357 cells in Figure 1D in Cancer Res. 2007b. Respondent reused and relabeled one image to represent multiple supershift assays done at different times for different experiments to show the effect of anti-NF-kB p65 antibody on NF-kB DNA-binding activity in: • Figure 2B in Cancer Res 2006a • Figure 5A in Cancer Res. 2007c Respondent reused and relabeled a second image to represent multiple supershift assays done at different times for different experiments to show the effect of anti-NF-kB p65 antibody on NF-kB DNA-binding activity in: • Figure 6D in Mol Cancer Ther. 2006 • Figure 4C in Cancer 2006 • Figure 3A in Cancer Res. 2006b • Figure 2C in Int J Cancer 2006 • Figure 1d in Int J Cancer 2008 Respondent reused and relabeled the Rb levels in multiple supershift assay figures representing different experiments done at different times. Respondent used the same loading control assay blots in the supershift assays that came from the EMSAs to show the effect of anti-NF-kB p65 antibody on NF-kB DNA-binding activity in: • Figure 6D in Mol Cancer Ther. 2006 • Figure 2B in Cancer Res. 2006a • Figure 4C in Cancer 2006 • Figure 3A (right) in Cancer Res. 2006b • Figure 2C in Int J Cancer 2006 • Figure 5A (right) in Cancer Res 2007c • Figure 1d (right) in Int J Cancer 2008 The institution revoked the Respondent’s Ph.D. degree and procured retractions or errata for all of the affected papers except Mol Cancer Ther. 2008. Dr. Wang entered into a Voluntary Exclusion Agreement (Agreement) and agreed to the following: E:\FR\FM\12AUN1.SGM 12AUN1 Federal Register / Vol. 85, No. 156 / Wednesday, August 12, 2020 / Notices (1) Respondent agreed to exclude himself voluntarily for a period of ten (10) years beginning on July 21, 2020, from any contracting or subcontracting with any agency of the United States Government and from eligibility for or involvement in nonprocurement programs of the United States Government referred to as ‘‘covered transactions’’ pursuant to HHS’s Implementation (2 CFR part 376) of OMB Guidelines to Agencies on Governmentwide Debarment and Suspension, 2 CFR part 180 (collectively the ‘‘Debarment Regulations’’); (2) Respondent agreed to exclude himself voluntarily from serving in any advisory capacity to PHS including, but not limited to, service on any PHS advisory committee, board, and/or peer review committee, or as a consultant for a period of ten (10) years, beginning on July 21, 2020; and (3) as a condition of the Agreement, Respondent will request that the following paper be corrected or retracted in accordance with 42 CFR 93.407(a)(1): • Mol. Cancer Ther. 2008 Feb;7(2):341–9 Dated: August 7, 2020. Elisabeth A. Handley, Director, Office of Research Integrity, Office of the Assistant Secretary for Health. [FR Doc. 2020–17602 Filed 8–11–20; 8:45 am] BILLING CODE 4150–31–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Institute on Aging; Notice of Closed Meeting khammond on DSKJM1Z7X2PROD with NOTICES Pursuant to section 10(d) of the Federal Advisory Committee Act, as amended, notice is hereby given of the following meeting. The meeting will be closed to the public in accordance with the provisions set forth in sections 552b(c)(4) and 552b(c)(6), Title 5 U.S.C., as amended. The grant applications and the discussions could disclose confidential trade secrets or commercial property such as patentable material, and personal information concerning individuals associated with the grant applications, the disclosure of which would constitute a clearly unwarranted invasion of personal privacy. Name of Committee: National Institute on Aging Special Emphasis Panel; AD Analysis. Date: September 4, 2020. Time: 2:00 p.m. to 5:00 p.m. Agenda: To review and evaluate grant applications. Place: National Institute on Aging, Gateway Building, 7201 Wisconsin Avenue, Bethesda, MD 20892 (Video Meeting). Contact Person: Nijaguna Prasad, Ph.D., Scientific Review Officer, Scientific Review Branch, National Institute on Aging, National Institutes of Health, 7201 Wisconsin Avenue, Gateway Building, Suite 2W200, Bethesda, VerDate Sep<11>2014 16:37 Aug 11, 2020 Jkt 250001 MD 20892, (301) 496–9667, nijaguna.prasad@nih.gov. (Catalogue of Federal Domestic Assistance Program Nos. 93.866, Aging Research, National Institutes of Health, HHS) Dated: August 6, 2020. Miguelina Perez, Program Analyst, Office of Federal Advisory Committee Policy. [FR Doc. 2020–17586 Filed 8–11–20; 8:45 am] BILLING CODE 4140–01–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health Fogarty International Center; Notice of Meeting Pursuant to section 10(d) of the Federal Advisory Committee Act, as amended, notice is hereby given of a meeting of the Fogarty International Center Advisory Board. The meeting will be open to the public, with attendance limited to space available. Individuals who plan to attend and need special assistance, such as sign language interpretation or other reasonable accommodations, should notify the Contact Person listed below in advance of the meeting. The meeting will be closed to the public in accordance with the provisions set forth in sections 552b(c)(4) and 552b(c)(6), Title 5 U.S.C., as amended. The grant applications and discussions could disclose confidential trade secrets or commercial property such as patentable material, and personal information concerning individuals associated with the grant applications, the disclosure of which would constitute clearly unwarranted invasion of personal privacy. Name of Committee: Fogarty International Center Advisory Board. Date: September 10–11, 2020. Closed: September 10, 2020, 12:00 p.m. to 3:00 p.m. Agenda: To review and evaluate grant applications. Place: Fogarty International Center, National Institutes of Health, 31 Center Drive, Bethesda, MD 20892 (Virtual Meeting). Open: September 11, 2020, 12:00 p.m. to 3:00 p.m. Agenda: Update and discussion of current and planned FIC activities. Place: Fogarty International Center, National Institutes of Health, 31 Center Drive, Bethesda, MD 20892 (Virtual Meeting). Meeting Access: https://www.fic.nih.gov/ About/Advisory/Pages/default.aspx. Contact Person: Kristen Weymouth, Executive Secretary, Fogarty International Center, National Institutes of Health, 31 Center Drive, Room B2C02, Bethesda, MD 20892–7952, (301) 496–1415, kristen.weymouth@nih.gov. PO 00000 Frm 00049 Fmt 4703 Sfmt 4703 48713 Any interested person may file written comments with the committee by forwarding the statement to the Contact Person listed on this notice. The statement should include the name, address, telephone number and when applicable, the business or professional affiliation of the interested person. Information is also available on the Institute’s/Center’s home page: https:// www.fic.nih.gov/About/Advisory/Pages/ default.aspx where an agenda and additional information for the meeting will be posted when available. (Catalogue of Federal Domestic Assistance Program Nos. 93.106, Minority International Research Training Grant in the Biomedical and Behavioral Sciences; 93.154, Special International Postdoctoral Research Program in Acquired Immunodeficiency Syndrome; 93.168, International Cooperative Biodiversity Groups Program; 93.934, Fogarty International Research Collaboration Award; 93.989, Senior International Fellowship Awards Program, National Institutes of Health, HHS) Dated: August 6, 2020. Miguelina Perez, Program Analyst, Office of Federal Advisory Committee Policy. [FR Doc. 2020–17589 Filed 8–11–20; 8:45 am] BILLING CODE 4140–01–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Human Genome Research Institute; Notice of Closed Meeting Pursuant to section 10(d) of the Federal Advisory Committee Act, as amended, notice is hereby given of the following meeting. The meeting will be closed to the public in accordance with the provisions set forth in sections 552b(c)(4) and 552b(c)(6), Title 5 U.S.C., as amended. The grant applications and the discussions could disclose confidential trade secrets or commercial property such as patentable material, and personal information concerning individuals associated with the grant applications, the disclosure of which would constitute a clearly unwarranted invasion of personal privacy. Name of Committee: Center for Inherited Disease Research Access Committee Grant Review. Date: September 11, 2020. Time: 11:30 a.m. to 2:30 p.m. Agenda: To review and evaluate grant applications. Place: National Human Genome Research Institute, National Institutes of Health, 6700B Rockledge Drive, Room 3185, Bethesda, MD 20892 (Telephone Conference Call). Contact Person: Barbara J. Thomas, Ph.D., Scientific Review Officer, Scientific Review Branch, National Human Genome Research E:\FR\FM\12AUN1.SGM 12AUN1

Agencies

[Federal Register Volume 85, Number 156 (Wednesday, August 12, 2020)]
[Notices]
[Pages 48709-48713]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2020-17602]


-----------------------------------------------------------------------

DEPARTMENT OF HEALTH AND HUMAN SERVICES

Office of the Secretary


Findings of Research Misconduct

AGENCY: Office of the Secretary, Health and Human Services (HHS).

ACTION: Notice.

-----------------------------------------------------------------------

SUMMARY: Findings of research misconduct have been made against Zhiwei 
Wang, M.D. (Respondent), former postdoctoral fellow, Department of 
Pathology, Karmanos Cancer Institute, Wayne State University (WSU). Dr. 
Wang engaged in research misconduct in research supported by U.S. 
Public Health Service (PHS) funds, specifically National Cancer 
Institute (NCI), National Institutes of Health (NIH), grants P20 
CA101936, P30 CA022453, R01 CA075059, R01 CA083695, R01 CA101870, R01 
CA109389, R01CA131151, R01 CA132794, and U19 CA113317. The 
administrative actions, including debarment for a period of ten (10) 
years, were implemented beginning on July 21, 2020, and are detailed 
below.

FOR FURTHER INFORMATION CONTACT: Elisabeth A. Handley, Director, Office 
of Research Integrity, 1101 Wootton Parkway, Suite 240, Rockville, MD 
20852, (240) 453-8200.

SUPPLEMENTARY INFORMATION: Notice is hereby given that the Office of 
Research Integrity (ORI) has taken final action in the following case:
    Zhiwei Wang, M.D., Wayne State University: Based on the report of 
an investigation conducted by WSU and additional analysis conducted by 
ORI in its oversight review, ORI found that Dr. Zhiwei Wang, former 
postdoctoral fellow, Department of Pathology, Karmanos Cancer 
Institute, WSU, engaged in research misconduct in research supported by 
PHS funds, specifically NCI, NIH, grants P20 CA101936, P30 CA022453, 
R01 CA075059, R01 CA083695, R01 CA101870, R01 CA109389, R01CA131151, 
R01 CA132794, and U19 CA113317.
    ORI found that Respondent engaged in research misconduct by 
knowingly, intentionally, and/or recklessly falsifying data that were 
included in grant applications R01 CA120008, R01 CA131151, and R01 
CA131456 submitted to NCI, NIH; his 2006 Ph.D. dissertation (hereafter 
referred to as the ``Dissertation''); and the following published 
papers:
     Activated K-Ras and INK4a/Arf deficiency promote 
aggressiveness of pancreatic cancer by induction of EMT consistent with 
cancer stem cell phenotype. J Cell Physiol. 2013 Mar;228(3):556-62 
(hereafter referred to as ``J Cell Physiol. 2013''). Erratum in: J Cell 
Physiol. 2014 Aug;229(8):1118. Retraction in: J Cell Physiol. 2016 
Oct;231(10):2304.
     Activated K-ras and INK4a/Arf deficiency cooperate during 
the development of pancreatic cancer by activation of Notch and NF-
[kappa]B signaling pathways. PLoS One 2011;6(6):e20537 (hereafter 
referred to as ``PLoS One 2011''). Erratum in: PLoS One 
2014;9(6):e101032. Retraction in: PLoS One. 2018 Oct 2;13(10):e0205289.
     Down-regulation of Notch-1 is associated with Akt and 
FoxM1 in inducing cell growth inhibition and apoptosis in prostate 
cancer cells. J Cell Biochem. 2011 Jan;112(1):78-88 (hereafter referred 
to as ``J Cell Biochem. 2011''). Retraction in: J Cell Biochem. 2016 
Aug;117(8):1962.
     Down-regulation of Notch-1 and Jagged-1 inhibits prostate 
cancer cell growth, migration and invasion, and induces apoptosis via 
inactivation of Akt, mTOR, and NF-[kappa]B signaling pathways. J Cell 
Biochem. 2010 Mar 1;109(4):726-36 (hereafter referred to as ``J Cell 
Biochem. 2010''). Retraction in: J Cell Biochem. 2016 Aug;117(8):1960.
     TW-37, a small-molecule inhibitor of Bcl-2, inhibits cell 
growth and invasion in pancreatic cancer. Int J Cancer 2008 Aug 
15;123(4):958-66 (hereafter referred to as ``Int J Cancer 2008''). 
Retraction in: Int J Cancer. 2016 Nov 1;139(9):2146.
     Induction of growth arrest and apoptosis in human breast 
cancer cells by 3,3-diindolylmethane is associated with induction and 
nuclear localization of p27kip. Mol Cancer Ther. 2008 Feb;7(2):341-9 
(hereafter referred to as ``Mol Cancer Ther. 2008'').
     Down-regulation of platelet-derived growth factor-D 
inhibits cell growth and angiogenesis through inactivation of Notch-1 
and nuclear factor-[kappa]B signaling. Cancer Res. 2007 Dec 1; 
67(23):11377-85 (hereafter referred to as ``Cancer Res.

[[Page 48710]]

2007c''). Retraction in: Cancer Res. 2018 Sep 15;78(18):5469.
     Down-regulation of Forkhead Box M1 transcription factor 
leads to the inhibition of invasion and angiogenesis of pancreatic 
cancer cells. Cancer Res. 2007 Sep 1;67(17):8293-300 (hereafter 
referred to as ``Cancer Res. 2007b''). Retraction in: Cancer Res. 2018 
Sep 15; 78(18):5470.
     Inhibition of angiogenesis and invasion by 3,3'-
diindolylmethane is mediated by the nuclear factor-[kappa]B downstream 
target genes MMP-9 and uPA that regulated bioavailability of vascular 
endothelial growth factor in prostate cancer. Cancer Res. 2007 Apr 
1;67(7):3310-9 (hereafter referred to as ``Cancer Res. 2007a''). 
Retraction in: Cancer Res. 2018 Sep 15; 78(18):5471.
     Notch-1 down-regulation by curcumin is associated with the 
inhibition of cell growth and the induction of apoptosis in pancreatic 
cancer cells. Cancer 2006 Jun 1;106(11):2503-13 (hereafter referred to 
as ``Cancer 2006''). Retraction in: Cancer 2016 Oct 15;122(20):3247.
     Epidermal growth factor receptor-related protein inhibits 
cell growth and invasion in pancreatic cancer. Cancer Res. 2006 Aug 
1;66(15):7653-60 (hereafter referred to as ``Cancer Res. 2006b''). 
Retraction in: Cancer Res. 2018 Sep 15;78(18):5474.
     Inhibition of nuclear factor kappa[beta] activity by 
genistein is mediated via Notch-1 signaling pathway in pancreatic 
cancer cells. Int J Cancer 2006 Apr 15;118(8):1930-6 (hereafter 
referred to as ``Int J Cancer 2006''). Erratum in: Int J Cancer 2014 
Apr 15;134(8):E3. Retraction in: Int J Cancer 2016 Nov 1;139(9):2145.
     Down-regulation of Notch-1 inhibits invasion by 
inactivation of nuclear factor-kappa[beta], vascular endothelial growth 
factor, and matrix metalloproteinase-9 in pancreatic cancer cells. 
Cancer Res. 2006 Mar 1;66(5):2778-84 (hereafter referred to as ``Cancer 
Res. 2006a''). Retraction in: Cancer Res. 2018 Sep 15;78(18):5476.
     Down-regulation of Notch-1 contributes to cell growth 
inhibition and apoptosis in pancreatic cancer cells. Mol Cancer Ther. 
2006 Mar;5(3):483-93 (hereafter referred to as ``Mol Cancer Ther. 
2006''). Retraction in: Mol Cancer Ther. 2018 Oct;17(10):2268.
    ORI found by a preponderance of evidence that Respondent engaged in 
research misconduct by intentionally, knowingly, and/or recklessly 
falsifying and/or fabricating images representing protein expression, 
invasion and migration assays, and electrophoretic mobility shift 
assays (EMSA) in experiments designed to identify underlying mechanisms 
controlling cell proliferation, differentiation, and apoptosis in 
cancer so that novel targeted therapeutic agents could be identified.
    Specifically, Respondent reused and relabeled:
     The same protein bands to represent experimental 
conditions in:

--Figure 6D (upper panel) in the Dissertation; Figure 1D (upper panel) 
in Mol Cancer Ther. 2006: Down-regulation of Notch-1 expression by 
siRNA in BxPC-3, HPAC, and PANC-1 cells
--Figure 6D (lower panel) in the Dissertation; Figure 1D (lower panel) 
in Mol Cancer Ther. 2006: Up-regulation of Notch-1 expression by cDNA 
transfection in BxPC-3, HPAC, and PANC-1 cells
--Figure 8A in Mol Cancer Ther. 2006: Down-regulation of Notch-1 
expression by genistein and Notch-1 siRNA
--Figure 4 in Int J Cancer 2006: Down-regulation of Notch-1 expression 
by genistein and Notch-1 siRNA

     inhibition of Bcl-XL (0-72 hours with 
genistein) in BxPC-3 cells in Figure 20 in the Dissertation, Figure 7B 
in Mol Cancer Ther. 2006, and Figure 3C in Int J Cancer 2006 to also 
represent:

--Inhibition of Bcl-XL (0-13 uM curcumin) in PANC-1 cells in 
Figure 3D in Cancer 2006
--inhibition of Notch-1 expression (ERRP and Notch-1 siRNA 
transfection) in BxPC-3 cells in Figure 5A in Cancer Res. 2006b

     inhibition of Hes-1 (0-72 hours genistein) in BxPC-3 cells 
in Figure 7B in Mol Cancer Ther. 2006 to also represent:

--Inhibition of Cyclin D1 (0-72 hours with genistein) in BxPC-3 cells 
in Figure 20 in the Dissertation and Figure 3C in Int J Cancer 2006
--inhibition of Cyclin D1 (0-13 uM curcumin in PANC-1 cells) in Figure 
3D in Cancer 2006
 inhibition of Cyclin D1 (0-72 hours with genistein) in BxPC-3 
cells in Figure 7B in Mol Cancer Ther. 2006 to also represent 
inhibition of Hes-1 (0-72 hours with genistein) in BxPC-3 cells in 
Figure 20 in the Dissertation and Figure 3C in Int J Cancer 2006
 expression of Bcl-2 in control and Notch-1 siRNA transfected 
pancreatic cell lines (BxPC-3, HPAC) in Figure 10 in the Dissertation 
and Figure 5 in Mol Cancer Ther. 2006 to represent expression of Notch-
1 in control and PDGF-D siRNA transfected pancreatic cells in Figure 4A 
in Cancer Res. 2007c.
 representing expression of Cyclin D1 and Bcl-XL in 
control and Notch-1 siRNA transfected pancreatic cell lines (BxPC-3, 
HPAC, PANC-1) in Figure 10 in the Dissertation and Figure 5D in Mol 
Cancer Ther. 2006 to represent expression of Hes-1 and Cyclin D1 in 
control and ERRP-incubated pancreatic cells in Figure 2C in Cancer Res. 
2006b
 expression of p27 in control and Notch-1 siRNA transfected 
pancreatic cell lines (HPAC) in Figure 10 in the Dissertation and 
Figure 5 in Mol Cancer Ther. 2006 to represent VEGF protein expression 
in control and Notch-1 plasmid transfected BxPC-3 cells in Figure 4B in 
Cancer Res. 2006a
 expression of Cyclin D1 in control and Notch-1 siRNA 
transfected pancreatic cell lines in Figure 10 in the Dissertation and 
Figure 5 in Mol Cancer Ther. 2006 to represent the expression of uPAR 
genes in control siRNA and FoxM1 siRNA transfected pancreatic cancer 
cells in Figure 5B in Cancer Res. 2007b
 expression of Hes-1 in control and ERRP-incubated pancreatic 
cancer cells in Figure 2C in Cancer Res. 2006b to represent the 
expression of uPAR genes in control siRNA and FoxM1 siRNA transfected 
pancreatic cancer cells in Figure 5B in Cancer Res. 2007b
 expression of Hes-1 in control and ERRP-incubated pancreatic 
cells in Figure 2C in Cancer Res. 2006b to represent control, TGF-
[alpha], and TGF-[alpha]+ERRP effects on Notch-1 activation in BxPC-3 
cells in Figure 2D in Cancer Res. 2006b
 inhibition of Bcl-XL, Hes-1, and Cyclin D protein 
expression by genistein in BxPC-3 cells at 0, 24, 48, and 72 hours in 
three different experiments in Figure 7B in Mol Cancer Ther. 2006 to 
represent the same protein expressions in one experiment in Figure 3C 
in Int J Cancer 2006
 up-regulation of Notch-1 in cDNA-transfected BxPC-3 cells in 
Figure 5C in Cancer Res. 2006b to also show that ERRP inhibits the 
expression of MMP-9 in Figure 6 in Cancer Res. 2006b
 expression of Notch-1 when transfected with Jagged-1 siRNA in 
PC-3 cells in Figure 5A in J Cell Biochem. 2010 to also show the 
expression of Notch-1 when transfected with Notch-1 siRNA in C4-2B 
cells in Figure 3A in J Cell Biochem. 2011
 expression of Notch-4 in a genetically modified mouse model 
(KCI) in Figure 1D in PLoS One 2011 to also

[[Page 48711]]

show the expression of Bcl-2 in the same mouse model in Figure 3A in 
the same paper
 expression of EZH2 in IC, KC, and KCI transgenic mice to also 
represent the expression of E-cadherin in the same mouse types in 
Figure 4B in J Cell Physiol. 2013

    Respondent reused and relabeled one set of [beta]-actin bands to 
represent loading controls for the following experiments showing:

 Inhibition of VEGF in Notch-1 siRNA transfected BxPC-3 cells 
in Figure 16B in the Dissertation
 inhibition of cyclin D1 in genistein-treated BxPC-3 
cells over time in Figure 7B in Mol Cancer Ther. 2006
 inhibition of Notch-1 in genistein-treated BxPC-3 cells over 
time in Figure 8A in Mol Cancer Ther. 2006
 down-regulation of MMP-9 expression in Notch-1 siRNA 
transfected BxPC-3 cells in Figure 17A (left) in the Dissertation and 
Figure 3B in Cancer Res. 2006a
 up-regulation by cDNA transfection and down regulation by 
Notch-1 siRNA transfection in BcPC-3 cells in Figure 4B in Cancer Res. 
2006a
 down-regulation of MMP-9 in ICN-transfected BxPC-3 cells in 
Figure 15B in the Dissertation and Figure 5A in Cancer Res. 2006a
 inhibition of Notch-1, Hes-1, Cyclin D1, and Bcl-XL 
protein expression after 72 hours of curcumin treatment in pancreatic 
cancer cells in Figure 3D in Cancer 2006
 down-regulation of Notch-1 expression by curcumin and Notch-1 
siRNA in Notch-1 siRNA-transfected BxPC-3 cells in Figure 5A in Cancer 
2006
 down-regulation of Notch-1 expression in Notch-1 siRNA-
transfected BxPC-3 cells compared with control in Figure 5A in Cancer 
Res. 2006b
 inhibition of Hes-1, Cyclin D1 and Bcl-xL in genistein-treated 
BxPC-3 cells over time in Figure 20C in the Dissertation and Figure 3C 
in Int J Cancer 2006
 inhibition of Bcl-xL, Bcl-2, Cyclin D1, COX-2, Survivin and 
MMP-9 protein expression by Notch-1 siRNA in BxPC-3 cells in Figure 6A 
in Int J Cancer 2006
 inhibition of IKK[alpha] and pI[kappa]B[alpha] protein 
expression by Notch-1 siRNA in BxPC-3 cells in Figure 6B in Int J 
Cancer 2006

    Respondent reused and relabeled a second set of [beta]-actin bands 
to represent loading controls for the following experiments showing:

 Increasing inhibition of Notch-1 by 25 [mu]mol/l genistein at 
24, 48, and 72 hours in BxPC-3 cells in Figure 20A in the Dissertation, 
Figure 7B in Mol Cancer Ther. 2006, and Figure 3A in Int J Cancer 2006
 up-regulation of Notch-1 in Notch-1 cDNA transfected BxPC-3 
cells, with or without 10 [mu]mol/l curcumin, in Figure 6A in Cancer 
2006

    Respondent reused and relabeled a third set of [beta]-actin bands 
to represent loading controls for the following experiments showing:

 The level of expression of seven known G0-
G1 cell cycle regulatory factors in Figure 10 in the 
Dissertation and Figure 5 in Mol Cancer Ther. 2006
 overexpression of Notch-1 in Notch-1 cDNA transfected BxPC-3 
cells in Figure 22A in the Dissertation and Figure 9A in Mol Cancer 
Ther. 2006
 inhibition of NF-[kappa]B target gene expression by Notch-1 
siRNA in BxPC-3 cells in Figure 23A in the Dissertation
 inhibition of IKK[alpha] and pI[kappa]B[alpha] protein 
expression by Notch-1 siRNA in BxPC-3 pancreatic cancer cells in Figure 
23B the Dissertation
 overexpression of Notch-1 in Notch-1 siRNA-transfected BxPC-3 
cells in Figure 1C in Cancer Res. 2006a
 down-regulation of VEGF by siRNA transfection in ICN-
transfected BxPC-3 cells in Figure 5A (right) in Cancer Res. 2006a
 up-regulation of Notch-1 in cDNA-transfected and cDNA and ERRP 
transfected BxPC-3 cells in Figure 5C in Cancer Res. 2006b
 inhibition of MMP-2, MMP-9, and uPAR genes by FoxM1 siRNA in 
BxPC-3, HPAC, and PANC-1 cells in Figure 5B in Cancer Res. 2007b

    Respondent reused and relabeled a fourth set of [beta]-actin bands 
to represent loading controls for the following experiments showing:

 FoxM1 expression in AsPC-1, BxPC-3, Colo-357, HPAC, L3.6pl, 
MIA PaCa and PANC-1 cells in Figure 1A in Cancer Res. 2007b
 PDGF-D expression in PDGF-D cDNA transfected BxPC-3, Colo-357, 
and MIA PaCa cells in Figure 2C in Cancer Res. 2007c
 Bcl-2 expression in AsPC-1, BxPC-3, Colo-357, HPAC, L3.6pl, 
MIA PaCa and PANC-1 cells in Figure 1C in Int J Cancer 2008

    Respondent reused and relabeled a fifth set of [beta]-actin bands 
to represent loading controls for the following experiments showing:

 Down regulation of PDFG-D expression by PDGF-D siRNA in BcPC-
3, HPAC, and Colo-357 cells and up-regulation of PDGF-D expression by 
PDGF-D cDNA in BxPC-3, Colo-357, and MIA PaCa cells in Figure 2C in 
Cancer Res. 2007c
 inhibition of Notch-1 expression by PDGF-D siRNA in BxPC-3, 
HPAC, and Colo-357 cells in Figure 4A in Cancer Res. 2007c

    Respondent reused and relabeled a sixth set of [beta]-actin bands 
to represent loading controls for the following experiments showing:

 Up-regulation of Notch-1 expression by cDNA in BxPC-3, HPAC, 
and PANC-1 cells in Figure 6D (bottom) in the Dissertation and Figure 
1D in Mol Cancer Ther. 2006
 down-regulation of Notch-1 expression by Notch-1 siRNA and 
genistein in BxPC-3 cells in Figure 21 in the Dissertation and Figure 
4A in Int J Cancer 2006

    Respondent reused and relabeled a seventh set of [beta]-actin bands 
to represent loading controls for the following experiments showing:

 Down-regulation of Notch-1 expression by Notch-1 siRNA in 
BxPC-3, HPAC, and PANC-1 cells in Figure 6D (top) in the Dissertation 
and Figure 1D in Mol Cancer Ther. 2006
 expression of Notch-1, Hes-1, and Cyclin D1 after incubation 
with recombinant ERRP in BxPC-3, HPAC, and PANC-1 cells in Figure 2C in 
Cancer Res. 2006b
 effects of ERRP, Erbitux, or Herceptin followed by exposure to 
TGF-[alpha] or HB-EGF on Notch-1 expression in BxPC-3 cells in Figure 
2D in Cancer Res. 2006b
 down-regulation of FoxM1 expression by FoxM1 siRNA in BxPC-3, 
HPAC, and PANC-1 cells in Figure 1D in Cancer Res. 2007b
 the level of expression of seven known G0-
G1 cell cycle regulatory factors (Survivin, cdc25A, p27, 
p21, Cyclin D1, Cyclin B, and CDK2) in Figure 4C in Cancer Res. 2007b

    Respondent reused and relabeled:

 Invasion assay results showing a high level of penetration of 
Notch-1 cDNA-transfected cells through a Matrigel matrix in Figure 1D 
in Cancer Res. 2006a, to also represent control siRNA-transfected cells 
(controls) not transfected with MMP-9 or VEGF siRNA in Figure 5B in 
Cancer Res. 2006a
 sections from one image of an invasion assay to show a lower 
level of penetration of C4-2B cells through a Matrigel matrix after 
treatment with 10 [micro]mol/L of B-DIM than in the control condition 
(DMSO) in Figure 6B in Cancer Res. 2007a

[[Page 48712]]

 sections from one image to show the penetration of both 
control and ERRP-treated HPAC cells through a Matrigel matrix in Figure 
4 in Cancer Res. 2006b
 one image to show the penetration of ERRP-treated PANC-1 cells 
through a Matrigel matrix in Figure 4 in Cancer Res. 2006b to also show 
the penetration of TW-37 treated Colo-357 cells in Figure 5b in Int J 
Cancer 2008
 images of assays of endothelial tube formation after HUVACs 
were trypsinized and seeded with control siRNA transfected BxPC-3 or 
HPAC cells in Figure 6c in Cancer Res. 2007b
 a single gel shift band showing the no treatment control 
condition (CS) in an EMSA assay using BxPC-3 cells showing down 
regulation of NF-[kappa]B DNA binding by Notch-1 siRNA in Figures 11A 
and 14A in the Dissertation to also show:

--The control conditions (CP) in assays showing activation of NF-
[kappa]B binding activity by Notch-1 plasmid (cDNA) transfection in 
Figures 11A and 14A in the Dissertation
--inhibition of NF-[kappa]B DNA binding activity after treatment with 
25 [mu]M genistein for 48 hours in Figure 19B in the Dissertation

 a single gel shift band showing the effect of Notch-1 siRNA 
transfection of BxPC-3 cells, showing inhibition of NF-[kappa]B DNA 
binding activity in Figures 11A and 14A in the Dissertation to also 
show NF-[kappa]B binding activity in BxPC-3 cells after treatment with 
25 [mu]M genistein in Figure 22C in the Dissertation
 a single gel shift band showing the effect of Notch-1 cDNA 
transfection of BxPC-3 cells, showing activation of NF-[kappa]B DNA 
binding activity in Figures 11A and 14A in the Dissertation to also 
show NF-[kappa]B binding activity in BxPC-3 cells in the no treatment 
control condition in an experiment showing the effect of genistein on 
binding in Figure 22C in the Dissertation
 a single gel shift band showing the no treatment control 
condition in an EMSA assay using HPAC cells showing down regulation of 
NF-[kappa]B DNA binding by Notch-1 siRNA in Figure 11A in the 
Dissertation to also show the no treatment control condition in the 
activation of NF-[kappa]B DNA binding after transfection with Notch-1 
cDNA

 a single gel shift band showing the effect of 0 [mu]M 
genistein on NF-[kappa]B binding activity in BxPC3 cells in Figure 19A 
the Dissertation to also show the effect of:

--25 [mu]M of genistein for 0 hours in HPAC cells in Figure 19B in the 
Dissertation
--Notch-1 cDNA on NF-[kappa]B binding activity in Figure 22C in the 
Dissertation

 a single gel shift band showing the effect of 10 [mu]M 
genistein on NF-[kappa]B binding activity in BxPC3 cells in Figure 19A 
in the Dissertation to also show the effect of:

--25 [mu]M genistein for 24 hours in HPAC cells in Figure 19B in the 
Dissertation
--Notch-1 cDNA plus 25 [mu]M genistein on NF-[kappa]B binding activity 
in Figure 22C in the Dissertation

 a single gel shift band showing the effect of Bcl-2 siRNA 
transfection of Colo-357 cells showing down-regulation of NF-[kappa]B 
DNA binding activity to also show the same effect with 500 nM TW-37 on 
Colo-357 cells in Figure 3a in Int J Cancer 2008

    Respondent reused and relabeled images representing the 
retinoblastoma control protein (Rb) levels from one EMSA in multiple 
figures. Respondent used the same loading controls assay blots, in 
different orders with some flipped horizontally, showing:

 Down-regulation of Notch-1 gene expression by Notch-1 siRNA in 
siRNA- and cDNA-transfected BxPC-3, HPAC, and PANC-1 cells in Figure 11 
in the Dissertation and Figure 6 in Mol Cancer Ther. 2006
 down-regulation of Notch-1 by genistein in BxPC-3 cells in 
Figure 7E in Mol Cancer Ther. 2006
 Notch-1 induced NF-[kappa]B DNA binding in Figure 14 in the 
Dissertation and Figure 2 in Cancer Res. 2006a
 down-regulation of Notch-1 by curcumin in BxPC-3 and PANC-1 
cells in Figures 4, 5D,
    and 6D in Cancer 2006
 inhibition of NF-[kappa]B activation in three types of 
pancreatic cancer cells (BxPC-3, HPAC, PANC-1) in Figure 3A in Cancer 
Res. 2006b
 inhibition of NF-[kappa]B DNA binding activity by genistein 
(by dose and time) in Figure 19 in the Dissertation and Figure 2 in Int 
J Cancer 2006
 inhibition of NF-[kappa]B DNA-binding activity by Notch-1 
siRNA in BxPC-3 pancreatic cancer cells in Figure 22 in the 
Dissertation and Figure 5 in Int J Cancer 2006
 decreased NF-[kappa]B DNA-binding activity through down-
regulation of PDGF-D by siRNA transfection in BxPC-3, HPAC, and Colo-
357 pancreatic cancer cells, activation of NF-[kappa]B DNA binding 
activity in BxPC3, Colo-357, and MIA PaCa pancreatic cancer cells in 
Figure 5A in Cancer Research 2007c
 differences in NF-[kappa]B activation in a panel of pancreatic 
cancer cell lines (AsPC-1, BxPC-3, Colo-357, HPAC, L3.6pl, MIA PaCa, 
PANC-1 in Figure 1d in Int J Cancer 2008
 inhibition of NF-[kappa]B activation by Bcl-2 siRNA in Colo-
357 cells and by TW-37 (by dose and time) in Colo-357 and BXPC-3 
pancreatic cancer cells in Figure 3a in Int J Cancer 2008
 inhibition of NF-[kappa]B activation by TW-37 in Colo-357 
tumor xenografts from SCID mice in Figure 6c in Int J Cancer 2008

    In addition, Respondent used these same images to represent [beta]-
actin in a figure showing that FoxM1 protein levels were up-regulated 
by FoxM1 cDNA plasmid in AsPC-1, PANC-1, and Colo-357 cells in Figure 
1D in Cancer Res. 2007b.
    Respondent reused and relabeled one image to represent multiple 
supershift assays done at different times for different experiments to 
show the effect of anti-NF-[kappa]B p65 antibody on NF-[kappa]B DNA-
binding activity in:

 Figure 2B in Cancer Res 2006a
 Figure 5A in Cancer Res. 2007c

    Respondent reused and relabeled a second image to represent 
multiple supershift assays done at different times for different 
experiments to show the effect of anti-NF-[kappa]B p65 antibody on NF-
[kappa]B DNA-binding activity in:

 Figure 6D in Mol Cancer Ther. 2006
 Figure 4C in Cancer 2006
 Figure 3A in Cancer Res. 2006b
 Figure 2C in Int J Cancer 2006
 Figure 1d in Int J Cancer 2008

    Respondent reused and relabeled the Rb levels in multiple 
supershift assay figures representing different experiments done at 
different times. Respondent used the same loading control assay blots 
in the supershift assays that came from the EMSAs to show the effect of 
anti-NF-[kappa]B p65 antibody on NF-[kappa]B DNA-binding activity in:

 Figure 6D in Mol Cancer Ther. 2006
 Figure 2B in Cancer Res. 2006a
 Figure 4C in Cancer 2006
 Figure 3A (right) in Cancer Res. 2006b
 Figure 2C in Int J Cancer 2006
 Figure 5A (right) in Cancer Res 2007c
 Figure 1d (right) in Int J Cancer 2008

    The institution revoked the Respondent's Ph.D. degree and procured 
retractions or errata for all of the affected papers except Mol Cancer 
Ther. 2008.
    Dr. Wang entered into a Voluntary Exclusion Agreement (Agreement) 
and agreed to the following:


[[Page 48713]]


    (1) Respondent agreed to exclude himself voluntarily for a 
period of ten (10) years beginning on July 21, 2020, from any 
contracting or subcontracting with any agency of the United States 
Government and from eligibility for or involvement in nonprocurement 
programs of the United States Government referred to as ``covered 
transactions'' pursuant to HHS's Implementation (2 CFR part 376) of 
OMB Guidelines to Agencies on Governmentwide Debarment and 
Suspension, 2 CFR part 180 (collectively the ``Debarment 
Regulations'');
    (2) Respondent agreed to exclude himself voluntarily from 
serving in any advisory capacity to PHS including, but not limited 
to, service on any PHS advisory committee, board, and/or peer review 
committee, or as a consultant for a period of ten (10) years, 
beginning on July 21, 2020; and
    (3) as a condition of the Agreement, Respondent will request 
that the following paper be corrected or retracted in accordance 
with 42 CFR 93.407(a)(1):

 Mol. Cancer Ther. 2008 Feb;7(2):341-9

    Dated: August 7, 2020.
Elisabeth A. Handley,
Director, Office of Research Integrity, Office of the Assistant 
Secretary for Health.
[FR Doc. 2020-17602 Filed 8-11-20; 8:45 am]
BILLING CODE 4150-31-P

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.